Rolstad B, Ford W L
Immunol Rev. 1983;73:87-113. doi: 10.1111/j.1600-065x.1983.tb01080.x.
Allogeneic lymphocyte cytotoxicity (ALC) refers to the destruction of lymphocyte beginning within a few hours of intravenous injection into non-sensitized, allogeneic recipients. Usually this has been detected in rats and mice by comparing the localization of 51Cr-labelled lymphocytes in the tissues of allogeneic and syngeneic recipients. In a particular strain combination the existence of ALC is supported by deficient localization of allogeneic lymphocytes in the LN, lungs and blood mononuclear population and an excess of the label that had been associated with allogeneic cells in the lymph plasma, blood plasma and kidneys. As the destruction of the allogeneic cells occurs in the lymphatic tissues, especially the spleen, it is paradoxical that there is sometimes an excess of the label associated with allogeneic cells in the spleen but evidence is presented that most of the isotope is no longer associated with living cells in that organ at 24 h after transfer. The data cannot be explained by an altered distribution of allogeneic lymphocytes between different organs. Experiments on the early migration of lymphocytes from the blood of syngeneic and allogeneic recipients point unequivocally to the conclusion that the adhesion of lymphocytes to specialized vascular endothelium in LN and their consequent entry into LN does not require that the lymphocytes and the endothelial cells share MHC products. The characteristics of ALC stressed in this review include the following: 1) it is independent of T-cell activation, either of host T-cells or of donor T-cells: 2) B- and T-cells are about equally vulnerable to ALC; 3) it varies greatly between different strain combinations regardless of other indices of cellular and humoral immunity; 4) F1 hybrid donor cells are vulnerable but the effect is always less marked than with allogeneic cells; 5) ALC is less radio-sensitive than primary cellular or humoral immune responses; 6) adoptive transfer of ALC can be achieved with TDL from nude rats. The possible mechanism underlying ALC has been debated in terms of natural killer cells recognizing certain allo-antigens or alternatively pre-existing "natural" antibody with low affinity for allogeneic cells leading to their elimination by ADCC. The argument hinges on the necessity for antibody and cannot be resolved by current data.
同种异体淋巴细胞毒性(ALC)是指在静脉注射到未致敏的同种异体受体后数小时内开始的淋巴细胞破坏。通常,在大鼠和小鼠中,通过比较51Cr标记的淋巴细胞在同种异体和同基因受体组织中的定位来检测这种情况。在特定的品系组合中,LN、肺和血液单核细胞群体中同种异体淋巴细胞的定位不足,以及淋巴血浆、血浆和肾脏中与同种异体细胞相关的标记物过量,支持了ALC的存在。由于同种异体细胞的破坏发生在淋巴组织,尤其是脾脏中,所以有时脾脏中与同种异体细胞相关的标记物会过量,但有证据表明,在转移后24小时,该器官中大多数同位素不再与活细胞相关,这是自相矛盾的。这些数据不能用同种异体淋巴细胞在不同器官之间分布的改变来解释。对来自同基因和同种异体受体血液中淋巴细胞早期迁移的实验明确指出,淋巴细胞与LN中特化血管内皮的粘附以及随后进入LN并不要求淋巴细胞和内皮细胞共享MHC产物。本综述强调的ALC特征如下:1)它独立于宿主T细胞或供体T细胞的T细胞激活;2)B细胞和T细胞对ALC的易感性大致相同;3)无论细胞免疫和体液免疫的其他指标如何,不同品系组合之间的差异很大;4)F1杂种供体细胞易受影响,但效果总是比同种异体细胞不明显;5)ALC比原发性细胞免疫或体液免疫反应对辐射的敏感性低;6)用裸鼠的TDL可以实现ALC的过继转移。关于ALC潜在的可能机制,存在着自然杀伤细胞识别某些同种异体抗原,或者存在对同种异体细胞亲和力低的预先存在的“天然”抗体,导致其被ADCC消除的争论。争论的关键在于抗体的必要性,目前的数据无法解决这个问题。